State Key Laboratory of Plant Physiology and Biochemistry, College of Life Sciences, Zhejiang University, Hangzhou, Zhejiang, 310058, China.
Division of Biochemistry, Interdisciplinary Plant Group, Bond Life Sciences Center, University of Missouri, Columbia, MO, 65211, USA.
Plant Cell Environ. 2018 Jan;41(1):134-147. doi: 10.1111/pce.12984. Epub 2017 Jul 5.
Ethylene, an important hormone in plant growth, development and response to environmental stimuli, is rapidly induced by mechanical injury or wounding. Although induction of ACS (1-aminocyclopropane-1-carboxylic acid synthase) gene expression has been associated with this process, the detailed regulatory mechanism is unclear. Here, we report that the wounding-induced ethylene production is modulated by both mitogen-activated protein kinase (MAPK) pathway and calcium-dependent protein kinase (CPK) pathway. Study using acs mutants demonstrated that four ACS isoforms, including ACS2, ACS6, ACS7 and ACS8, contribute to ethylene production in response to wounding. Loss-of-function analysis defines the role of MPK3 and MPK6, and their upstream MKK4 and MKK5, in wounding-induced ethylene production. They play an important role in the wounding-induced up-regulation of all four ACS genes expression. Independent of MAPK pathway, CPK5 and CPK6 are also involved in the wounding-induced ethylene production by regulating the expression of ACS2, ACS6 and ACS8 genes. Taken together, we demonstrate that two independent kinase signalling pathways, MPK3/MPK6 cascade and CPK5/CPK6, are involved in the wounding-induced ethylene biosynthesis via differential regulation of ACS genes at transcriptional level.
乙烯是植物生长、发育和对环境刺激反应的重要激素,它会被机械损伤或创伤迅速诱导。虽然 ACS(1-氨基环丙烷-1-羧酸合酶)基因表达的诱导与这一过程有关,但详细的调控机制尚不清楚。在这里,我们报告称,MAPK(丝裂原活化蛋白激酶)途径和钙依赖性蛋白激酶(CPK)途径调节了创伤诱导的乙烯生成。使用 acs 突变体的研究表明,四种 ACS 同工型,包括 ACS2、ACS6、ACS7 和 ACS8,有助于对创伤的乙烯生成反应。功能丧失分析定义了 MPK3 和 MPK6 及其上游 MKK4 和 MKK5 在创伤诱导的乙烯生成中的作用。它们在创伤诱导的所有四种 ACS 基因表达的上调中发挥重要作用。独立于 MAPK 途径,CPK5 和 CPK6 也通过调节 ACS2、ACS6 和 ACS8 基因的表达参与创伤诱导的乙烯生成。总之,我们证明了两条独立的激酶信号通路,即 MPK3/MPK6 级联和 CPK5/CPK6,通过在转录水平上对 ACS 基因进行差异化调节,参与了创伤诱导的乙烯生物合成。